Learn a new dance, movement , language to grow new brain cells

Surround yourself with people who will let you get the optimum potential that your brain can do to be successful in your own terms. You control your destiny, what your career will be , your finances and happiness.

Find an inspiration. I want to be a doctor before I reached the age of 80. I will use the internet for free skills and knowledge while I save for the time to be full time student as Nurse Practitioner first.

Every time we learn a new dance, movement , language or reach new accomplishments and solve new challenges, our brain cells grow.

So, grow your brain cells and be in control. Do not use the excuse that someone introduced you to a path that later on is a failure. Use that failure to get up and do a meaningful project you own and be proud of. I believe in the human potential and the power of the mind to control the brain to move and do some learning.

Connie

motor neurons

HUMAN SKIN CELLS TRANSFORMED INTO MOTOR NEURONS

WUSTL researchers have converted skin cells into motor neurons without going through the stem cell state. The new technique could help in the development of devastating neurodegenerative diseases, like ALS, that affect motor neurons. READ MORE…
Image shows a neuron.

ROBOTIC SYSTEM MONITORS SPECIFIC NEURONS

Researchers have developed a robotic system that allows them to focus in on specific neurons in the brain. The technology could help answer questions such as how neurons interact with each other as we recall a memory. READ MORE…

Nurture is every influence from without that affects man after his birth

Summary: A new study reveals a diverse array of genetic changes that occur in the brain following sensory experiences.

Source: Harvard.

“Nature and nurture is a convenient jingle of words, for it separates under two distinct heads the innumerable elements of which personality is composed. Nature is all that a man brings with himself into the world; nurture is every influence from without that affects him after his birth.” – Francis Galton, cousin of Charles Darwin, 1874.

Is it nature or nurture that ultimately shapes a human? Are actions and behaviors a result of genes or environment? Variations of these questions have been explored by countless philosophers and scientists across millennia. Yet, as biologists continue to better understand the mechanisms that underlie brain function, it is increasingly apparent that this long-debated dichotomy may be no dichotomy at all.

In a study published in Nature Neuroscience on Jan. 21, neuroscientists and systems biologists from Harvard Medical School reveal just how inexorably interwoven nature and nurture are in the mouse brain. Using novel technologies developed at HMS, the team looked at how a single sensory experience affects gene expression in the brain by analyzing more than 114,000 individual cells in the mouse visual cortex before and after exposure to light.

Their findings revealed a dramatic and diverse landscape of gene expression changes across all cell types, involving 611 different genes, many linked to neural connectivity and the brain’s ability to rewire itself to learn and adapt.

The results offer insights into how bursts of neuronal activity that last only milliseconds trigger lasting changes in the brain, and open new fields of exploration for efforts to understand how the brain works.

“What we found is, in a sense, amazing. In response to visual stimulation, virtually every cell in the visual cortex is responding in a different way,” said co-senior author Michael Greenberg, the Nathan Marsh Pusey Professor of Neurobiology and chair of the Department of Neurobiology at HMS.

“This in essence addresses the long-asked question about nature and nurture: Is it genes or environment? It’s both, and this is how they come together,” he said.

One out of many

Neuroscientists have known that stimuli–sensory experiences such as touch or sound, metabolic changes, injury and other environmental experiences–can trigger the activation of genetic programs within the brain.

Composed of a vast array of different cells, the brain depends on a complex orchestra of cellular functions to carry out its tasks. Scientists have long sought to understand how individual cells respond to various stimuli. However, due to technological limitations, previous genetic studies largely focused on mixed populations of cells, obscuring critical nuances in cellular behavior.

To build a more comprehensive picture, Greenberg teamed with co-corresponding author Bernardo Sabatini, the Alice and Rodman W. Moorhead III Professor of Neurobiology at HMS, and Allon Klein, assistant professor of systems biology at HMS.

Spearheaded by co-lead authors Sinisa Hrvatin, a postdoctoral fellow in the Greenberg lab, Daniel Hochbaum, a postdoctoral fellow in the Sabatini lab and M. Aurel Nagy, an MD-PhD student in the Greenberg lab, the researchers first housed mice in complete darkness to quiet the visual cortex, the area of the brain that controls vision.

They then exposed the mice to light and studied how it affected genes within the brain. Using technology developed by the Klein lab known as inDrops, they tracked which genes got turned on or off in tens of thousands of individual cells before and after light exposure.

The team found significant changes in gene expression after light exposure in all cell types in the visual cortex–both neurons and, unexpectedly, nonneuronal cells such as astrocytes, macrophages and muscle cells that line blood vessels in the brain.

Roughly 50 to 70 percent of excitatory neurons, for example, exhibited changes regardless of their location or function. Remarkably, the authors said, a large proportion of non-neuronal cells–almost half of all astrocytes, for example–also exhibited changes.

The team identified thousands of genes with altered expression patterns after light exposure, and 611 genes that had at least two-fold increases or decreases.

Many of these genes have been previously linked to structural remodeling in the brain, suggesting that virtually the entire visual cortex, including the vasculature and muscle cell types, may undergo genetically controlled rewiring in response to a sensory experience.

There has been some controversy among neuroscientists over whether gene expression could functionally control plasticity or connectivity between neurons.

“I think our study strongly suggests that this is the case, and that each cell has a unique genetic program that’s tailored to the function of a given cell within a neural circuit,” Greenberg said.

Question goldmine

These findings open a wide range of avenues for further study, the authors said. For example, how genetic programs affect the function of specific cell types, how they vary early or later in life and how dysfunction in these programs might contribute to disease, all of which could help scientists learn more about the fundamental workings of the brain.

“Experience and environmental stimuli appear to almost constantly affect gene expression and function throughout the brain. This may help us to understand how processes such as learning and memory formation, which require long-term changes in the brain, arise from the short bursts of electrical activity through which neurons signal to each other,” Greenberg said.

brainbow of the cerebral cortex

One especially interesting area of inquiry, according to Greenberg, includes the regulatory elements that control the expression of genes in response to sensory experience. In a paper published earlier this year in Molecular Cell, he and his team explored the activity of the FOS/JUN protein complex, which is expressed across many different cell types in the brain but appears to regulate unique programs in each different cell type.

Identifying the regulatory elements that control gene expression is critical because they may account for differences in brain function from one human to another, and may also underlie disorders such as autism, schizophrenia and bipolar disease, the researchers said.

“We’re sitting on a goldmine of questions that can help us better understand how the brain works,” Greenberg said. “And there is a whole field of exploration waiting to be tapped.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Additional authors on the study include Marcelo Cicconet, Keiramarie Robertson, Lucas Cheadle, Rapolas Zilionis, Alex Ratner and Rebeca Borges-Monroy.

Funding: This work was supported by the National Institutes of Health (R01NS028829, R01NS046579, T32GM007753, R33CA212697, 5T32AG000222-23), F. Hoffmann-La Roche Ltd., the William F. Milton Fund, a Burroughs Wellcome Fund Career Award and an Edward J. Mallinckrodt Scholarship.

Source: Ekaterina Pesheva – Harvard
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Lichtman Lab, Harvard University.
Original Research: Abstract in Nature Neuroscience.
DOI:10.1038/s41593-017-0029-5

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Harvard “Nature, Meet Nurture.” NeuroscienceNews. NeuroscienceNews, 8 February 2018.
<http://neurosciencenews.com/genetic-nature-experience-8455/&gt;.

Abstract

Single-cell analysis of experience-dependent transcriptomic states in the mouse visual cortex

Activity-dependent transcriptional responses shape cortical function. However, a comprehensive understanding of the diversity of these responses across the full range of cortical cell types, and how these changes contribute to neuronal plasticity and disease, is lacking. To investigate the breadth of transcriptional changes that occur across cell types in the mouse visual cortex after exposure to light, we applied high-throughput single-cell RNA sequencing. We identified significant and divergent transcriptional responses to stimulation in each of the 30 cell types characterized, thus revealing 611 stimulus-responsive genes. Excitatory pyramidal neurons exhibited inter- and intralaminar heterogeneity in the induction of stimulus-responsive genes. Non-neuronal cells showed clear transcriptional responses that may regulate experience-dependent changes in neurovascular coupling and myelination. Together, these results reveal the dynamic landscape of the stimulus-dependent transcriptional changes occurring across cell types in the visual cortex; these changes are probably critical for cortical function and may be sites of deregulation in developmental brain disorders.

 


Connie’s comments:

I massaged my babies after birth before each bath and even up to now when they are sick. I train all caregivers to massage home-bound older adults or seniors needing 24/7 care.

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Snapshots of Life: The Birth of New Neurons

Radial Glia in Oil

Snapshots of Life: The Birth of New Neurons

After a challenging day at work or school, sometimes it may seem like you are down to your last brain cell. But have no fear—in actuality, the brains of humans and other mammals have the potential to produce new neurons throughout life. This remarkable ability is due to a specific type of cell—adult neural stem cells—so beautifully highlighted in this award-winning micrograph.

Here you see the nuclei (purple) and arm-like extensions (green) of neural stem cells, along with nuclei of other cells (blue), in brain tissue from a mature mouse. The sample was taken from the subgranular zone of the hippocampus, a region of the brain associated with learning and memory. This zone is also one of the few areas in the adult brain where stem cells are known to reside.

Kira Mosher, a postdoctoral fellow in the NIH-supported lab of Dave Schaffer at the University of California, Berkeley, captured this striking image using a confocal microscope. Then, to make it really pop, Mosher used photo-editing software to add a few “oil painting” effects. For her efforts, the micrograph was named a winner in the UC Berkeley 2017 MIC Image Contest.

Images like this one are helping the Schaffer lab pinpoint the locations of neural stem cells and map their interactions with other cells, providing clues to their potential roles in health and disease.The researchers also plan to use CRISPR gene-editing tools to tinker with neural stem cells and learn more about the molecular signals needed for them to function normally.

As scientists gain a more detailed view, the hope is they’ll be in a better position to figure out how to transplant or activate neural stem cells for possible use in brain repair. Such research might lead to new strategies for helping people with stroke, Alzheimer’s disease, Parkinson’s disease, and other conditions in which neurons are lost.

 Links:

Focus on Stem Cell Research (National Institute of Neurological Disorders and Stroke/NIH)

Schaffer Lab (University of California, Berkeley)

NIH Support: National Eye Institute; National Institute of General Medical Sciences; National Institute of Neurological Disorders and Stroke

Lending Late Neurons a Helping Hand

All kinds of positive and loving stimulation of the newborn using massage, breastfeeding, and other forms of communication help in growing neurons.

Connie


 

Lending Late Neurons a Helping Hand

Summary: Delayed neural migration in fetuses may cause behavioral disorders similar to autism, researchers report.

Source: University of Geneva.

During the foetal stage, millions of neurons are born in the walls of the ventricles of the brain before migrating to their final location in the cerebral cortex. If this migration is disrupted, the new-born baby may suffer serious consequences, including intellectual impairment. What happens, however, if the migration takes place but is delayed?

Researchers at the University of Geneva (UNIGE), Switzerland, have discovered that even a slight delay may lead to behavioural disorders that are similar to autistic characteristics in human. Furthermore, they found that these disorders are due to the abnormally low activity of the late neurons, which leads to permanent deficit of interneuronal connections.

neurons

The Geneva neuroscientists succeeded in correcting the activity of the relevant neurons, thereby restoring the missing connections and preventing the appearance of behavioural disorders.

The results, which are published in the journal Nature Communications, will open up new avenues for preventing neurodevelopmental disorders linked to the cerebral cortex.

Neurons at the foetal stage are generated in the walls of the brain’s ventricles before migrating to their final destination in the cerebral cortex between the sixth and sixteenth week of pregnancy in women. This migration is governed by numerous molecular signals that control the tempo of this movement so that neurons arrive at the right place at the right time. If this migration is permanently disrupted, the new-born infant could suffer mental deficiencies or epileptic seizures, for example. But what happens if neurons arrive at the right place but are delayed?

The importance of punctuality for creating neural connections

“To find an answer, we manipulated in utero the Wnt signalling pathways which regulates the pace of migration in a few thousand rat neurons, begins Jozsef Kiss, professor in the Department of Basic Neuroscience at UNIGE’s Faculty of Medicine, so that the neurons are positioned appropriately but late. We then checked that they were in the right place and conducted various behaviour tests on the rats once they became adult”. The neuroscientists made two discoveries: not only did the rats exhibit sociability problems but they also developed repeated compulsive behaviours – both of which are symptoms related to autism in humans. But how can the late arrival of just a few thousand neurons out of millions disrupt brain function to such a degree?

“When we marked the late neurons,” continues professor Kiss, “we observed that they receive fewer fibres and, as a result, create fewer synaptic contacts with the other neurons compared to a ‘punctual’ neuron. This lack of connections leads to a decrease in neuronal activity, which ultimately has an impact on the interactions and connectivity between the left and right hemispheres of the brain”. The late neurons, since they are poorly connected at the outset, establish fewer contacts with their counterparts in the other hemisphere. During the post-natal period in rats, the neurons only have ten or so days to develop these connections between the two hemispheres: hence the impact of a delay of a few days on the development of the brain and the resulting behavioural consequences.

Making up for lost time!

The UNIGE researchers subsequently explored the possibility of catching up on the time lost by the neurons that did not migrate on schedule by stimulating their activity remotely. “We added a gene to the late neurons so that we could control the neuronal activity remotely. We stimulated them when we wanted to in order to try to make up for the delay and subsequent lack of activity. And it worked!” says Kiss. In fact, thanks to the remote activation ‘therapy’, the researchers found that the connections between the two hemispheres were formed correctly and that no behavioural disorders appeared in the adult rats. “But it has to be done during the critical period,” adds Kiss. “In other words, during the ten days postnatally; when the inter-hemispheric connections develop in the rats. The activation of neurons after this so-called “critical period” will not rescue normal connectivity and behaviour.”

The neuroscientists at UNIGE have demonstrated for the first time that, although a brain may be formed normally, it can malfunction due to delayed neuronal migration. This handful of badly integrated neurons appear sufficient to disrupt communication between the two hemispheres of the brain, inducing behavioural problems. More surprisingly, we now know that the effects of migration delay on the connectivity can be reversed if the neuronal activity is stimulated externally in a controlled manner during the critical period of axon development. As Professor Kiss concludes: “We can now think of ways of detecting a delay in interhemispheric connections and devise ‘activation therapies’ at clinical level to prevent the behavioural problems observed in neurodevelopmental disorders such as autism.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Jozsef Kiss – University of Geneva
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Bocchi et al. Nature Communication 2017.
Original Research: Full open access research for “Perturbed Wnt signaling leads to neuronal migration delay, altered interhemispheric connections and impaired social behavior” by Riccardo Bocchi, Kristof Egervari, Laura Carol-Perdiguer, Beatrice Viale, Charles Quairiaux, Mathias De Roo, Michael Boitard, Suzanne Oskouie, Patrick Salmon & Jozsef Z. Kiss in Nature Communications. Published online October 27 2017 doi:10.1038/s41467-017-01046-w

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Geneva “Lending Late Neurons a Helping Hand.” NeuroscienceNews. NeuroscienceNews, 7 November 2017.
<http://neurosciencenews.com/neural-migration-behavior-7896/&gt;.

Abstract

Perturbed Wnt signaling leads to neuronal migration delay, altered interhemispheric connections and impaired social behavior

Perturbed neuronal migration and circuit development have been implicated in the pathogenesis of neurodevelopmental diseases; however, the direct steps linking these developmental errors to behavior alterations remain unknown. Here we demonstrate that Wnt/C-Kit signaling is a key regulator of glia-guided radial migration in rat somatosensory cortex. Transient downregulation of Wnt signaling in migrating, callosal projection neurons results in delayed positioning in layer 2/3. Delayed neurons display reduced neuronal activity with impaired afferent connectivity causing permanent deficit in callosal projections. Animals with these defects exhibit altered somatosensory function with reduced social interactions and repetitive movements. Restoring normal migration by overexpressing the Wnt-downstream effector C-Kit or selective chemogenetic activation of callosal projection neurons during a critical postnatal period prevents abnormal interhemispheric connections as well as behavioral alterations. Our findings identify a link between defective canonical Wnt signaling, delayed neuronal migration, deficient interhemispheric connectivity and abnormal social behavior analogous to autistic characteristics in humans.

“Perturbed Wnt signaling leads to neuronal migration delay, altered interhemispheric connections and impaired social behavior” by Riccardo Bocchi, Kristof Egervari, Laura Carol-Perdiguer, Beatrice Viale, Charles Quairiaux, Mathias De Roo, Michael Boitard, Suzanne Oskouie, Patrick Salmon & Jozsef Z. Kiss in Nature Communications. Published online October 27 2017 doi:10.1038/s41467-017-01046-w

Chewing and brain growth: Reduced Mastication Impairs Memory and Learning Function

Summary: Researchers find changes in masticatory stimuli can modulate neurogenesis and hippocampal function. Published in the Journal of Dental Research, findings reveal reduced mastication impaired learning and memory function in mice.

Source: Tokyo Medical and Dental University

According to researchers, the frequency of mastication has dramatically decreased along with changes in dietary habits. Masticatory stimulation has influence on the development of the central nervous system as well as the growth of maxillofacial tissue in children. Deterioration of masticatory function due to aging and the consequent reduction of brain function has become major problems. Although the relationship between mastication and brain function is potentially important, the mechanism underlying is not fully understood.

In order to prevent brain function disorders, including those relating to memory and learning, it is an urgent task to elucidate the linkage between masticatory function and brain function.

Researchers found that growth of the maxillofacial bone and muscle were suppressed in mice with reduced masticatory stimuli by feeding with powder food. In addition, behavioral experiments revealed that reduced mastication impaired memory and learning functions. In the hippocampus, a major component responsible for memory, neural activity, synapse formation and expression of brain-derived neurotrophic factor (BDNF) were reduced in these mice .

Thus, the authors demonstrated that the changes in masticatory stimuli can modulate neurogenesis and neuronal activity in the hippocampus, functionally contributing to cognitive function.

This research suggests that maintaining or strengthening of masticatory function would be effective in preventing dementia and memory/learning dysfunction. It is also suggested that further elucidation of the mechanism linking mastication and brain function can lead to novel treatments and preventive measures for memory/learning dysfunction in the future.

 Image shows hippocampal neurons.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Japan Agency for Medical Research and Development, Japan Science and Technology Agency, Ministry of Education, Culture, Sports, Science and Technology funded this study.

Source: Takashi Ono – Tokyo Medical and Dental University
Image Source: NeuroscienceNews.com image is credited to Department of Cell Signaling,Department of Orthodontic Science (TMDU).
Original Reserch: Abstract for “Reduced Mastication Impairs Memory Function” by Y. Fukushima-Nakayama, Takehito Ono, M. Hayashi, M. Inoue, H. Wake, Takashi Ono, and T. Nakashima in Journal of Dental Research. Published online June 16 doi:10.1177/0022034517708771

Tokyo Medical and Dental University “Chew On This: Reduced Mastication Impairs Memory and Learning Function.” NeuroscienceNews. NeuroscienceNews, 10 July 2017.
<http://neurosciencenews.com/mastication-memory-learning-7052/&gt;.

Abstract

Reduced Mastication Impairs Memory Function

Mastication is an indispensable oral function related to physical, mental, and social health throughout life. The elderly tend to have a masticatory dysfunction due to tooth loss and fragility in the masticatory muscles with aging, potentially resulting in impaired cognitive function. Masticatory stimulation has influence on the development of the central nervous system (CNS) as well as the growth of maxillofacial tissue in children. Although the relationship between mastication and cognitive function is potentially important in the growth period, the cellular and molecular mechanisms have not been sufficiently elucidated.

Here, we show that the reduced mastication resulted in impaired spatial memory and learning function owing to the morphological change and decreased activity in the hippocampus.

We used an in vivo model for reduced masticatory stimuli, in which juvenile mice were fed with powder diet and found that masticatory stimulation during the growth period positively regulated long-term spatial memory to promote cognitive function.

The functional linkage between mastication and brain was validated by the decrease in neurons, neurogenesis, neuronal activity, and brain-derived neurotrophic factor (BDNF) expression in the hippocampus.

These findings taken together provide in vivo evidence for a functional linkage between mastication and cognitive function in the growth period, suggesting a need for novel therapeutic strategies in masticatory function–related cognitive dysfunction.

“Reduced Mastication Impairs Memory Function” by Y. Fukushima-Nakayama, Takehito Ono, M. Hayashi, M. Inoue, H. Wake, Takashi Ono, and T. Nakashima in Journal of Dental Research. Published online June 16 doi:10.1177/0022034517708771

Sleep scientists’ wake-up call for later school starts

  • student sleeping on a desk

As they prepare a major study to test the idea, UK scientists have said that starting school at 10:00 could have huge benefits for teenagers.

Research suggests that society pays too little attention to our “body clock” – and adolescents in particular have a late-running biological rhythm.

This means insisting on an early start can cause sleep deprivation, which in turn can affect learning and health.

A sleep expert made the argument at the British Science Festival in Bradford.

Dr Paul Kelley said that adolescents effectively lose up to two hours of sleep per day, which is “a huge society issue”.

He and colleagues from Oxford are leading a project called Teensleep, which is currently recruiting 100 schools from around the UK to take part in what Dr Kelley called “the world’s largest randomised control trial”, due to commence in 2016.

Ups and downs

Our body clock is a daily cycle which drives the regular rise and fall of certain genes as well as the ebb and flow of our cognitive performance, our metabolism and so on.

For much of our lives – and especially in adolescence – there is a mismatch between this rhythm and the typical working day.

In fact, Dr Kelley said, the body clock of most people between age 10 and 55 is not well suited to rising early.

“Most people wake up to alarms, because they don’t naturally wake up at the time when they have to get up and go to work.

“So we’ve got a sleep deprived society – it’s just that this age group, say 14-24 in particular, is more deprived than any other sector.”

Dr Kelley and his colleagues, including well-known Oxford sleep researcher Prof Russell Foster, argue that school days should start at 10:00 and university at 11:00, to better match the circadian rhythms of adolescents and young adults.

“All the evidence points to the same thing,” Dr Kelley told BBC News.

“There are no negative outcomes for moving [the school day] later, no positive outcomes for moving earlier.”

Silhoutted head watching a screen

The Teensleep experiment, which is funded by the Wellcome Trust and the Education Endowment Fund, will randomly assign its 100 schools into four groups.

One group of schools will shift their school days for 14- to 16-year-olds to a 10:00 start; another group will offer “sleep education” to their students.

This involves “helping students and staff realise sensible ways of making their sleep good sleep”, Dr Kelley said, such as avoiding screen-based activity in the evening.

A third group of schools will introduce both a later start and sleep education, while a fourth, control group will make no such changes.

Keenly awaited

The interventions will commence in the 2016-17 academic year, and the researchers plan to report their results in 2018.

city nightscapeThe availability of artificial light has shifted humans’ daily rhythm

Derk-Jan Dijk is a professor of sleep and physiology at the University of Surrey. He cautioned that shifting the school day might be of limited use without changing other habits that affect our sleep, especially night-time light exposure – making the education part of the trial particularly important.

“It is clear that these adolescents tend to drift later. And many of them will probably prefer to start later,” he told the BBC.

“But why do adolescents like to sleep in later and go to bed later? What is causing this?

“There is undoubtedly a biological component, but that interacts with our artificial light environment.

“And if we can’t change that, then is delaying school times the best solution? Because that way you might not solve the problem – you might shift them even later.”

Prof Dijk said the Teensleep experiment was an important one, which he would observe with interest.

“It will be very interesting to see the results.”


What’s stopping my slumber?

Sleep

A lack of sleep has been linked to weight gain, depression and reduced fertility.